LINKÖPING, Sweden — The sex hormone estrogen could be the reason more women than men suffer from an irregular heartbeat — also called an arrhythmia. Although women generally have better protection against cardiovascular diseases than men, this is not the case when it comes to hereditary diseases causing an abnormal heart rhythm.
Researchers from Linköping University in Sweden looked at one particular disease called Long QT syndrome LQTS), in which the heart takes longer than normal to finish every heartbeat. This syndrome is most often due to a congenital hereditary change, or mutation, affecting one of the heart’s ion channels. It’s relatively rare, affecting around one in 2,500 people.
Ion channels are small pores that go through the cell’s membranes and regulate the flow of electrically charged ions in and out of the cell. Some ion channels act as an accelerator and others as a brake. Together, they regulate every one of the 2.5 billion heartbeats most of us have during our entire lifetimes.
“We’re trying to understand which substances in the body impact the function of the ion channels. If we could figure out how this regulation works, maybe we can understand why some individuals are more protected and others are hit harder,” says Sara Liin, associate professor in the Department of Biomedical and Clinical Sciences at LiU, in a media release.
Only estrogen had an impact on ion channels
Using frogs’ eggs, the team inserted the human variant of the ion channel into the eggs which do not have this channel. They added the most active form of the sex hormone estrogen, called estradiol, and measured the ion channel function.
It turned out that estrogen hampered ion channel function, which indicates that the hormone may increase the risk of certain types of arrhythmia. Other sex hormones had no effect.
The research, published in the journal Science Advances, also discovered exactly which parts of the channel estrogen affected.
Study author then further examined ion channel mutations found in families with hereditary arrhythmia syndromes. Some mutations led to high estrogen sensitivity, while others led to the ion channel completely losing estrogen sensitivity.
“We show that some hereditary mutations that reduce ion channel function seem to contribute to high estrogen sensitivity, so there could be two risk factors that interact especially in women carriers of these mutations. We believe that our study gives good reason to look closer at this in patients,” Liin explains.
The researchers point out that it is important to remember the many positive effects of estrogen. For women with a hereditary increased risk of LQTS, however, estrogen could possibly be a risk factor.
South West News Service writer Jim Leffman contributed to this report.